急性心包炎心电图特征性改变的诊断价值

心包脏层和壁层的急性炎症为心包炎，病因很多。临床上常以听到心包摩擦音和（或）有心包积液而诊断，据报道约90％的患者可有心电图异常。本文旨在探讨急性心包炎时P—R段偏移及ST／T比值特异性的临床诊断价值。     

中心静脉导管留置治疗结核性心包积液的临床评价

目的 探讨中心静脉导管留置引流在治疗结核性心包炎伴有大量心包积液的应用价值.方法 将76例结核性渗出性心包炎患者随机分为A组和B组,均予以全身规则抗结核治疗.A组留置中心静脉导管引流及心包腔内注药,B组常规心包穿刺抽液及心包腔内注药.结果 A组与B组相比,两组间在消除心包填塞症状时间,退热时间,心包积液消失时间等方面有显著性差异（P＜0.01）.结论 心包穿刺留置导管引流心包积液安全可行,操作简便,可迅速消除心包填塞症状,能及时彻底引流心包积液,疗效明显,降低了缩窄性心包炎的发生率.     

透析相关性心包炎14例报告

尿毒症性心包炎经充分血液透析常可得到缓解,然而心包疾患又常并发于慢性血液透析过程中.多数学者称此为透析相关性心包炎。现将我院进行慢性血液透析过程中发生相关性心包炎患者14例的临床资料报告如下. 一般资料血液透析患者81例,透析期间发生心包积液者14例(占12%).男8例,女6例.慢性肾炎者10例,慢性肾孟肾炎2例,多囊肾和梗阻性肾病各1例,维持性透析时间为94～328个透析日,出现心包炎的平均时间为116个透析日. 临床     

中心静脉导管留置治疗结核性心包积液的临床评价

目的探讨中心静脉导管留置引流在治疗结核性心包炎伴有大量心包积液的应用价值。方法将76例结核性渗出性心包炎患者随机分为A组和B组,均予以全身规则抗结核治疗。A组留置中心静脉导管引流及心包腔内注药,B组常规心包穿刺抽液及心包腔内注药。结果A组与B组相比,两组间在消除心包填塞症状时间,退热时间,心包积液消失时间等方面有显著性差异(P＜ 0．01)。结论心包穿刺留置导管引流心包积液安全可行,操作简便,可迅速消除心包填塞症状,能及时彻底引流心包积液,疗效明显,降低了缩窄性心包炎的发生率。     

尿毒症透析患者心包炎的临床研究

本文回顾性分析了近５年中９６例行维持性血液透析的慢性肾衰患者临床资料。确诊心包炎者１３例，发生率为１４％，其中尿毒症性心包炎８例，透析相关性心包炎５例。前者与机体过度水负荷有关，与ＢＵＮ升高无关，低蛋白血症是尿毒症心包积液形成的辅因，后者与高β２微球蛋白及中分子物质（ＭＭＳ）血症及肝素用量有关。尿毒症心包炎的治疗以限不、脱水、提高胶体渗透压及强化透析为主，血滤?血液透析滤过及减少肝素用量有助于治疗     

留置中心静脉导管治疗结核性心包积液30例的临床分析

我国结核性心包炎在心包疾病中占有重要的位置,占心包疾病的21．3％～35．8％,高于国外。结核性心包积液患者若积液量较多或增长较快引起心包填塞症状时,需行心包穿刺抽液治疗,常规心包穿刺抽液容易损伤血管、心脏,风险较大。我院2000年以来收治的30例中等量以上结核性心包积液患者行中心静脉导管（Central Venous Catheter,CVC）留置引流心包积液,效果满意,现报告如下。     

急性心包炎心电图表现的若干新概念

临床上急性心包炎常以听到心包摩擦音和(或)有心包积液而作出诊断，约90％的患者可有心电图异常，其中以ST段抬高及PR段偏移较为特异。本文旨在探讨急性心包炎心电图表现的若干新概念，着重讨论PR段偏移的特性及其临床意义。     

留置中心静脉导管治疗结核性心包积液30例的临床分析

我国结核性心包炎在心包疾病中占有重要的位置,占心包疾病的21.3%～35.8%,高于国外.结核性心包积液患者若积液量较多或增长较快引起心包填塞症状时,需行心包穿刺抽液治疗,常规心包穿刺抽液容易损伤血管、心脏,风险较大.我院2000年以来收治的30例中等量以上结核性心包积液患者行中心静脉导管（Central Venous Catheter，CVC）留置引流心包积液，效果满意，现报告如下。[第一段]     

加强透析治疗尿毒症心包炎的预期效果

自Bright1836年首先描述尿毒症性心包炎以来,本症一直是肾脏疾病的一种致命的并发症,现在如处理得当,通常治疗有效。本文观察了98例有尿毒症性心包炎的慢性肾衰患者,均有典型的心包摩擦音,心包填塞的血液动力学证据,或通过手术或尸解证实为尿毒症性心包炎。除1例后来死于与心包炎无关者外,67例对加强血液透析(每周至少5次)或持续性腹膜透析有反应,心包炎消失。30例对透析无反应,其中8例在手术前死于心包炎的血液动力学并发症,22例需要手术治疗(急性心包填塞10例,加强透析后再发生低血压2例,心包积液增多或变化不大10例)。手术前加强透析的平     

恶性心包间皮瘤误诊1例

患者女,47岁,因胸闷、心前区不适6个月,加重1个月而入院。3个月前,患者曾在本院诊断为心包炎、心包积液,经心包穿刺抽液及辅助检查,心包炎性质不明确,经抗痨治疗好转出院。1个月前因症状加重,在外院B超检查发现心包腔内     

Pericardial involvement in end-stage renal disease

Pericardial involvement in end-stage renal disease (ESRD) is manifested most commonly as acute uremic or dialysis pericarditis and infrequently as chronic constrictive pericarditis. The causes of uremic and dialysis pericarditis remain uncertain. The clinical and laboratory manifestations of acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis in patients with chronic renal failure are similar to those observed in nonuremic patients with similar pericardial involvement, except that chest pain occurs less frequently in those with ESRD. Therapeutic interventions for acute uremic or dialysis pericarditis with or without pericardial effusion include intensive hemodialysis, pericardiocentesis (infrequently used), pericardiostomy with or without instillation of intrapericardial glucocorticoids, pericardial window, and pericardiectomy. Chronic constrictive pericarditis is treated with pericardiectomy.     

Etiology and prognostic implications of a large pericardial effusion in men

To assess the etiology and prognosis of a large pericardial effusion, we reviewed 25 consecutive patients who presented with a large pericardial effusion and underwent a drainage procedure. Large pericardial effusion was defined as: (1) an echo-free space greater than or equal to 10 mm anteriorly and posteriorly by M-mode echocardiography and (2) removal of greater than or equal to 350 ml of fluid at pericardial drainage. The etiologies of large pericardial effusion were: neoplastic (36%), idiopathic (32%), uremic (20%), postmyocardial infarction (8%), and acute rheumatic fever (4%). Of our patients, 44% presented with cardiac tamponade, while 25% of patients with idiopathic pericarditis had hemorrhage effusion and cardiac tamponade. At follow-up, 37 +/- 17 months after pericardial drainage, 68% had died from complications of their underlying disease. There were no deaths attributed to pericardial disease. While 88% of patients with idiopathic large pericardial effusion were alive at follow-up, none of the neoplastic large pericardial effusion patients survived longer than 5 months after initial pericardial drainage (p less than 0.001). Additionally, the survival of patients with uremic large pericardial effusion was better than patients with neoplastic large pericardial effusion (p less than 0.05). We conclude: (1) neoplastic, idiopathic, and uremic pericarditis are the most common causes of large pericardial effusion in men, (2) idiopathic pericarditis can be hemorrhagic and cause cardiac tamponade, and (3) the prognosis of large pericardial effusion is related to patients' underlying disease.     

Uremic pericarditis as a cause of cardiac tamponade.

Uremic pericarditis may complicate either acute or, more commonly, chronic renal failure. When dialysis is not employed, uremic pericarditis is usually a preterminal event and is characterized by a serofibrinous exudation of an amount inadequate to cause cardiac tamponade. Nevertheless, cardiac tamponade may uncommonly be observed in nondialyzed patients. Cardiac tamponade, which may be life-threatening, is more common in dialyzed than in nondialyzed patients with chronic renal failure. The primary causes of cardiac tamponade in uremic pericarditis in order of decreasing frequency are (1) pericardial effusion, usually of the serosanguineous type, (2) massive hemorrhage into the pericardial sac and (3) collagenization of pericardial exudate. From pathologic evidence, the following forms of therapy appear appropriate to manage uremic pericarditis that has reached the stage of causing cardiac tamponade. For effusion, pericardiocentesis or parietal pericardiectomy are logical procedures. Massive hemorrhage into the pericardial sac is usually attended by clotting and requires pericardiotomy and evacuation of clot. Collagenization of exudate yields an encasing, fibrous shell over the heart and requires decortication, as is practised in classical constrictive pericarditis.     

Uremic pericarditis complicating cardiac tamponade: a case report

A 29-year-old man developed diabetes mellitus in 1983 and diabetic nephropathy which gradually worsened from 1998. He was admitted to our hospital for initiation of peritoneal dialysis in May 2002. However, the efficiency of dialysis was not sufficient to improve elevated levels of blood urea nitrogen and serum creatinine. His body weight and cardiothoracic index by chest roentgenography gradually increased starting 9 days after admission. To improve the efficiency of dialysis, we tried to increase the dialysis fluid. Nevertheless, the efficiency of peritoneal dialysis remained low, and the patient complained of nausea 14 days after admission. Hypotension suddenly occurred 16 days after admission. Echocardiography showed massive pericardial effusion and collapse of the right ventricle. The diagnosis was cardiac tamponade. We performed cardiac centesis and pericardial drainage which revealed bloody pericardial effusion. Urgent hemodialysis was performed. The differential diagnosis of cardiac tamponade was established. After hemodialysis, the amount of pericardial effusion decreased, the gastro-intestinal symptoms disappeared, and the blood urea nitrogen and serum creatinine levels decreased. We speculated that the cause of cardiac tamponade was uremic pericarditis after ruling out infectious disease, collagen disease, malignant disease, and aortic dissection. Cardiac tamponade due to uremic pericarditis has become very rare since hemodialysis was developed.     

Pericarditis in end-stage renal disease

Our approach to the clinical management of uremic and dialysis-associated pericarditis has been presented previously and is outlined in Figure 1. In hemodynamically stable patients with no effusion and in those with small to medium effusions, we recommend initial therapy with intensified dialysis. Close monitoring, perhaps every third day, with echocardiography should be carried out. If pericardial effusion progressively increases or if a large pericardial effusion fails to resolve after 7 to 10 days of intensive dialysis, the pericardial effusion may be drained by subxiphoid pericardiotomy or by pericardiectomy. Similarly, if hemodynamic evidence of cardiac pretamponade or tamponade appears, surgical drainage also should be carried out. If the echocardiogram is inadequate for interpretation but tamponade physiology is present, we recommend confirmation by cardiac catheterization before surgical drainage is attempted, recognizing that there may be circumstances such as left ventricular failure and pulmonary hypertension that may complicate the interpretation of the catheterization data. The type of invasive pericardial procedure chosen is determined by local experience. As stated, we prefer not to perform pericardiocentesis before surgery unless tamponade-induced hypotension is so severe that an adequate blood pressure cannot be maintained by means of plasma volume expansion. Under these circumstances, we prefer that pericardiocentesis be performed in the operating room immediately before the induction of anesthesia for the definitive surgical procedure. Although pericardiectomy is a definitive procedure for pericarditis with effusion in the uremic patient, the procedure has substantial morbidity. The results of subxiphoid pericardiotomy are encouraging, and it is clear that it can be carried out safely in patients who are debilitated or who are at increased risk from general anesthesia and major surgery.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pericarditis: differential diagnostic considerations.

A retrospective analysis of 133 patients was performed to define the factors identifying those individuals at risk for the more serious causes of pericardial disease. In 90% of the cases, the initial assessment from data obtained without pericardiocentesis or pericardiectomy proved correct. Underlying tuberculous or maligant pericarditis were the most common sources of error on initial assessment. Hemodynamic compromise exclusive of anticoagulants, roentgenographic cardiomegaly, pleural effusion, low voltage on ECG, and large pericardial effusion by echocardiography were more common (P less than .05) in tuberculous pericarditis than in acute idiopathic pericarditis. We discuss similar risk factors in patients with chronic idiopathic, rheumatologic, and uremic pericarditis. Anterior pericardiectomy is favored as the diagnostic procedure of choice in patients at risk for the more serious causes of pericarditis because of greater safety, diagnostic sensitivity, and potential therapeutic benefit.     

Predicting success of intensive dialysis in the treatment of uremic pericarditis

To identify predictors of the success or failure of daily intensive dialysis in uremic pericarditis, a retrospective examination was made of initial clinical, laboratory, and echocardiographic data in 97 patients using univariate and multivariate statistical analysis. In this group, 67 patients showed response to intensive dialysis, and 30 patients did not (22 required surgery and eight died). By univariate analysis, nine factors correlated with intensive dialysis failure (p < 0.10): admission temperature over 102 °F, rales, admission blood pressure under 100 mm Hg, jugular venous distension, peritoneal dialysis treatment only because of severe hemodynamic instability, white blood cell count over 15,000/mm³, white blood cell count left shift, large effusion by echocardiography, and both anterior and posterior effusion by echocardiography. Echocardiographic left ventricular size and function were not useful predictors of success or failure; there was no difference in response to hemodialysis in patients with pericarditis before dialysis (69 percent) versus patients with pericarditis during a maintenance program (67 percent). By discriminant analysis, a seven-variable function was constructed that divided the patients into three groups: (1) those likely to show response to intensive dialysis (48 patients, predictive value of 98 percent), (2) those with an intermediate (38 percent) chance of showing response to intensive dialysis (30 patients), and (3) those unlikely to show response to intensive dialysis (14 patients, predictive value of 100 percent). When the function was applied prospectively to 12 patients (eight with success and four with failure), all were classified correctly. Thus, discriminant analysis of patients with uremic pericarditis allows improved selection of patients with uremic pericarditis likely to have response to daily intensive dialysis and early consideration of alternative forms of treatment in patients unlikely to show response to intensive dialysis. However, the model should be validated in the particular institution where it is to be used before its application.     

T wave changes consistent with epicardial involvement in acute myocardial infarction: Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis

Objectives. This study was designed to evaluate the presence or absence of atypical T wave evolution in patients with a postinfarclion pericardial effusion but without clinically recognized postinfarction pericarditis. A second purpose was to evaluate the frequency of atypical T wave evolution in a previous study of postinfarction pericarditis.Background. Electrocardiographic (ECG) criteria involving the evolution of the T wave after an acute myocardial infarction were recently described in patients with regional postinfarction pericarditis. Atypical T wave evolution was found to have a sensitivity of 100% and a specificity of 77% for clinically recognized regional postinfarction pericarditis with or without a pericardial effusion.Methods. The hospital records and serial ECGs of 20 patients with clinically recognized postinfarction pericarditis (Group I) were reviewed. The records and serial ECGs of 20 additional patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis (Group II) were also examined. The type of postinfarction T wave pattern, typical or atypical, was recorded in both groups.Results. All 20 patients in Group I had atypical T wave evolution. Among the 20 patients in Group II, every patient also had atypical T wave evolution. Fifteen percent of all 40 patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred postinfarction pericarditis.Conclusions. The high sensitivity of atypical T wave evolution in diagnosing regional postinfarction pericarditis was confirmed. However, similar T wave alterations were also observed when a postinfarction pericardial effusion existed in the absence of clinically recognized pericarditis. Fifteen percent of patients with atypical T wave evolution had a non-Q wave infarction with definite or inferred pericardial involvement. Thus, the presence of atypical T wave evolution may be a more sensitive indicator of a transmural infarction than the development of a Q wave.     

Pericardioscopy--a new window to the heart in inflammatory heart diseases]

Pericardioscopy is a new diagnostic tool to visualize macroscopically alterations of both the epicardium and pericardium. For the first time the macropathology of the epicarditis and pericarditis can be observed in vivo by the cardiologist in viral, bacterial, uremic and autoimmune cardiac processes. It enables us also to get an insight into neoplastic and metastatic processes affecting the heart and the pericardium. The prerequisite is the documentation of a larger pericardial (greater than 150 ml by the cubic model) effusion with an echocardiographically documented effusion of type C (Figure 1b), which must have at least 5 mm separation of the epicardial and pericardial layer in diastole at the anterior side of the heart when echocardiographic imaging is performed from the subxyphoidal or third intercostal space (Figure 1a). The first experience in 30 patients is reported. After puncture of the pericardial effusion a 9F sheath was introduced by use of a guide wire under echocardiographic and/or x-ray control (Figure 3). The fluid was removed by aspiration and 100 to 150 ml of body warm saline were infused in the pericardial sack. A flexible 8F fiber glass instrument (Vantec, Baxter or Storz) and a rigid 110 degrees 8F endoscope (Storz) were used for visualization of peri- and epicardium and for video documentation (Figure 2). After endoscopic inspection of the macropathology fibrinous strands (Figure 4) or increased vascular injection (Figure 5) can be observed in viral, autoimmune or idiopathic pericarditis or perimyocarditis. In the latter three forms of pericardial effusion only inflammatory cells (Figure 6) can be observed when the pericardial fluid is analyzed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Large pericardial effusions of inflammatory origin in childhood

OBJECTIVES: Our aim was to review the clinical records from children with large pericardial effusions of inflammatory origin presenting to a tertiary referral centre over the last 21 years, with emphasis on their clinical presentation, management and outcome. BACKGROUND: The common identifiable causes of pericardial effusion in children include prior cardiac surgery, bacterial pericarditis, malignancy, and connective tissue disorders. In a significant number of children, however, despite extensive investigation, it is not possible to identify a clear aetiology. A viral cause is often considered, though rarely confirmed. The clinical course of such large idiopathic pericardial effusions in children has not been extensively reported. METHODS AND RESULTS: We reviewed retrospectively the records of all patients seen between 1981 and 2001 with large pericardial effusions of inflammatory origin requiring drainage, excluding the effusions related to cardiac surgery or malignancy. We found 31 patients fulfilling our criterions for study. They could be divided into three groups, with 15 patients having no specific identifiable aetiology despite extensive investigation, 12 patients having evidence of bacterial pericarditis, and four with a probable immunologic disorder. Fever was present in only eight patients (53%) in the idiopathic group. All patients in the other groups had fever. Except for fever and the resultant tachycardia, it was not possible to distinguish on clinical grounds, nor on the presence or otherwise of cardiac tamponade, between those with idiopathic aetiology and those with bacterial infection. Of the patients with presumed bacterial pericarditis, five (42%) had both positive blood and pericardial fluid cultures, three (25%) had positive blood cultures, while a further three patients (25%) had only positive pericardial fluid cultures. All patients required drainage of the pericardial effusion, either under echocardiographic guidance or surgically. None of the patients died. The hospital stay was significantly shorter for those with idiopathic as opposed to bacterial pericarditis. Of those with an idiopathic aetiology, six required readmission due to recurrence of the pericardial effusion, with four patients requiring further surgical drainage. No patients required readmission with a bacterial or immunologic aetiology. No patient developed constrictive pericarditis after a median follow-up of 22 months. CONCLUSION: Patients with large idiopathic pericardial effusion had relatively few constitutional symptoms as compared with their gross echocardiographic findings. Those with bacterial pericarditis had more urgent need for treatment. Patients with pericardial effusion of inflammatory origin, when treated appropriately, had an excellent outcome with no mortality or development of constrictive pericarditis.